Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells

Brian D. Lamon; Barbara D. Summers; Antonio M. Gotto; David P. Hajjar

doi:10.1016/j.ejphar.2008.12.047

Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells

Brian D. Lamon, Barbara D. Summers, Antonio M. Gotto, David P. Hajjar

Research output: Contribution to journal › Article › peer-review

8 Scopus citations

Abstract

Statins have been demonstrated to elicit a broad range of cellular events resulting in an attenuation of the inflammatory response and enhanced protection to the components of the vessel wall. The present study was designed to examine the effect of pitavastatin on pathways associated with the proinflammatory gene, early growth response (Egr)-1, in human vascular smooth muscle cells. Pretreatment with pitavastatin resulted in a dose-dependent reduction in Egr-1 protein and suppressed Egr-1 mRNA expression in response to phorbol 12-myristate 13-acetate (PMA). A reduction in Egr-1 expression reduced the activation of NGFI-A binding protein (NAB)-2, an Egr-1-dependent gene. Furthermore, these events appeared to be dependent on the ability of pitavastatin to attenuate signaling cascades associated with extracellular regulated kinase (ERK) 1/2, but not p38 and c-Jun N-terminal kinase (JNK).

Original language	English (US)
Pages (from-to)	72-76
Number of pages	5
Journal	European Journal of Pharmacology
Volume	606
Issue number	1-3
DOIs	https://doi.org/10.1016/j.ejphar.2008.12.047
State	Published - Mar 15 2009

Keywords

Early growth response (Egr)-1
Mitogen-activated protein kinase (MAPK)
Smooth muscle cells
Statins

ASJC Scopus subject areas

Pharmacology

Access to Document

10.1016/j.ejphar.2008.12.047

Cite this

@article{363264237d7c48cf9d12ee1140848fb2,

title = "Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells",

abstract = "Statins have been demonstrated to elicit a broad range of cellular events resulting in an attenuation of the inflammatory response and enhanced protection to the components of the vessel wall. The present study was designed to examine the effect of pitavastatin on pathways associated with the proinflammatory gene, early growth response (Egr)-1, in human vascular smooth muscle cells. Pretreatment with pitavastatin resulted in a dose-dependent reduction in Egr-1 protein and suppressed Egr-1 mRNA expression in response to phorbol 12-myristate 13-acetate (PMA). A reduction in Egr-1 expression reduced the activation of NGFI-A binding protein (NAB)-2, an Egr-1-dependent gene. Furthermore, these events appeared to be dependent on the ability of pitavastatin to attenuate signaling cascades associated with extracellular regulated kinase (ERK) 1/2, but not p38 and c-Jun N-terminal kinase (JNK).",

keywords = "Early growth response (Egr)-1, Mitogen-activated protein kinase (MAPK), Smooth muscle cells, Statins",

author = "Lamon, {Brian D.} and Summers, {Barbara D.} and Gotto, {Antonio M.} and Hajjar, {David P.}",

note = "Funding Information: This work was supported by a sponsored research agreement with Kowa Co, Ltd, Tokyo, Japan, and in part, by a National Institutes of Health (NIH) T32 training grant in vascular biology (NIH HL-07423, awarded to Dr. David P. Hajjar). Drs. David P. Hajjar and Antonio M. Gotto Jr. are consultants for Kowa Pharmaceuticals in the area of atherosclerosis research. We would also like to acknowledge the late Dr. Tucker Collins from the Department of Pathology at the Children's Hospital in Boston, MA, for his contributions towards the initiation of this project.",

year = "2009",

month = mar,

day = "15",

doi = "10.1016/j.ejphar.2008.12.047",

language = "English (US)",

volume = "606",

pages = "72--76",

journal = "European Journal of Pharmacology",

issn = "0014-2999",

publisher = "Elsevier B.V.",

number = "1-3",

}

TY - JOUR

T1 - Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells

AU - Lamon, Brian D.

AU - Summers, Barbara D.

AU - Gotto, Antonio M.

AU - Hajjar, David P.

N1 - Funding Information: This work was supported by a sponsored research agreement with Kowa Co, Ltd, Tokyo, Japan, and in part, by a National Institutes of Health (NIH) T32 training grant in vascular biology (NIH HL-07423, awarded to Dr. David P. Hajjar). Drs. David P. Hajjar and Antonio M. Gotto Jr. are consultants for Kowa Pharmaceuticals in the area of atherosclerosis research. We would also like to acknowledge the late Dr. Tucker Collins from the Department of Pathology at the Children's Hospital in Boston, MA, for his contributions towards the initiation of this project.

PY - 2009/3/15

Y1 - 2009/3/15

N2 - Statins have been demonstrated to elicit a broad range of cellular events resulting in an attenuation of the inflammatory response and enhanced protection to the components of the vessel wall. The present study was designed to examine the effect of pitavastatin on pathways associated with the proinflammatory gene, early growth response (Egr)-1, in human vascular smooth muscle cells. Pretreatment with pitavastatin resulted in a dose-dependent reduction in Egr-1 protein and suppressed Egr-1 mRNA expression in response to phorbol 12-myristate 13-acetate (PMA). A reduction in Egr-1 expression reduced the activation of NGFI-A binding protein (NAB)-2, an Egr-1-dependent gene. Furthermore, these events appeared to be dependent on the ability of pitavastatin to attenuate signaling cascades associated with extracellular regulated kinase (ERK) 1/2, but not p38 and c-Jun N-terminal kinase (JNK).

AB - Statins have been demonstrated to elicit a broad range of cellular events resulting in an attenuation of the inflammatory response and enhanced protection to the components of the vessel wall. The present study was designed to examine the effect of pitavastatin on pathways associated with the proinflammatory gene, early growth response (Egr)-1, in human vascular smooth muscle cells. Pretreatment with pitavastatin resulted in a dose-dependent reduction in Egr-1 protein and suppressed Egr-1 mRNA expression in response to phorbol 12-myristate 13-acetate (PMA). A reduction in Egr-1 expression reduced the activation of NGFI-A binding protein (NAB)-2, an Egr-1-dependent gene. Furthermore, these events appeared to be dependent on the ability of pitavastatin to attenuate signaling cascades associated with extracellular regulated kinase (ERK) 1/2, but not p38 and c-Jun N-terminal kinase (JNK).

KW - Early growth response (Egr)-1

KW - Mitogen-activated protein kinase (MAPK)

KW - Smooth muscle cells

KW - Statins

UR - http://www.scopus.com/inward/record.url?scp=61449119630&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=61449119630&partnerID=8YFLogxK

U2 - 10.1016/j.ejphar.2008.12.047

DO - 10.1016/j.ejphar.2008.12.047

M3 - Article

C2 - 19374880

AN - SCOPUS:61449119630

SN - 0014-2999

VL - 606

SP - 72

EP - 76

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

IS - 1-3

ER -

Pitavastatin suppresses mitogen activated protein kinase-mediated Erg-1 induction in human vascular smooth muscle cells

Abstract

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this